Norepinephrine Noradrenergic systems

Ethanol also reduces the activity of the noradrenergic system in the locus coeruleus, and alterations in norepinephrine activity may account for some aspects of intoxication and the abstinence syndrome. The 0.2 antagonist clon-idine and the P-receptor antagonist propranolol reduce some symptoms of alcohol withdrawal (Bailly et al. 1992 Carlsson and Fasth 1976 Dobrydnjov et al. 2004 Kahkonen 2003 Petty et al. 1997 Wong et al. 2003). 

McCormick, DA, Pape, HC and Williamson, A (1991) Actions of norepinephrine in the cerebral cortex and thalamus implications for function of the central noradrenergic system. Prog. Brain Res. 88 293-305. 

What then, is the current evidence to support a role of norepinephrine in depression, such that manipulation of noradrenergic activity bears particular relevance to the successful treatment of mood disorders Interpretation of studies depends on the continually evolving conceptualizations of the roles of brain noradrenergic systems. A potentially useful way of thinking about the function of the norepinephrine in the brain can be derived from examining the neuroanatomy of the noradrenergic system. A summary of findings [primarily from rodents and primates) is as follows. 

Neuronal systems that contain one of the monoamines—norepinephrine, dopamine, or 5-hydroxytryptamine (serotonin)— provide examples in this category. Certain other pathways emanating from the reticular formation and possibly some peptide-containing pathways also fall into this category. These systems differ in fundamental ways from the hierarchical systems, and the noradrenergic systems serve to illustrate the differences. 

Drs. Peter Kirsch and Andreas Meyer-Lindenberg from Mannheim, Germany, are experts on the prosocial neuropeptide oxytocin and discuss its role in humans and its relevance for autism pathogenesis and therapy. In the chapter The Role of the Noradrenergic System in Autism Spectrum Disorders , Dr. David Beversdorf presents the normal role of norepinephrine and its effects on cognition and the possible dysregulation of norepinephrine in autism and possible treatment with propanolol. 

In brain slices, even though no anesthesia is present, there is a reduction in both noradrenergic and other inputs to these cells (e.g., from sensory systems) thus most of these neurons become silent. Consistent with this interpretation is the fact that all presumed serotonergic neurons we have tested in the brain slice are uniformly activated by norepinephrine or the < ragonist phenylephrine, applied either iontophoretically or in the perfusion medium (51). Similarly, in... 

Capuano CA, Leibowitz SF, Barr GA. 1992. The pharmaco-ontogeny of the paraventricular alpha 2-noradrenergic receptor system mediating norepinephrine-induced feeding in the rat. Brain Res Dev Brain Res 68(1) 67-74. 

Dextroamphetamine is a powerful stimulant of the nervous system that manifests its effects by releasing dopamine and norepinephrine from presynaptic nerve endings, thus stimulating central dopaminergic and noradrenergic receptors. In certain doses it strengthens the excitatory process in the CNS, reduces fatigue, elevates mood and the capacity to work, reduces the need for sleep, and decreases appetite. 

Angiotensin II, acting at presynaptic receptors on noradrenergic nerve terminals, potentiates the release of norepinephrine during low-frequency sympathetic nerve stimulation. Aside from its action on the nerve terminals of postganglionic sympathetic neurons, angiotensin II can directly stimulate sympathetic neurons in the central nervous system, in peripheral autonomic ganglia, and at the adrenal medulla. 

A number of theories have been put forward to account for the hypotensive action of a-methyldopa. Current evidence suggests that for a-methyldopa to be an antihypertensive agent, it must be converted to a-methyl-norepinephrine however, its site of action appears to be in the brain rather than in the periphery. Systemically administered a-methyldopa rapidly enters the brain, where it accumulates in noradrenergic nerves, is converted to a-methylnorepinephrine, and is released. Released a-methylnorepinephrine activates CNS a-adrenoceptors whose function is to decrease sympathetic outflow. Why a-methylnorepinephrine decreases sympathetic outflow more effectively than does the naturally occurring transmitter is not entirely clear. 

Mirtazapine (Remeron) enhances both serotonergic and noradrenergic neurotransmission. By blocking presynaptic aj-adrenoceptors, mirtazapine causes release of norepinephrine. Indirectly, through noradrenergic modulation of serotonin systems, mirtazapine also causes increased release of serotonin. It is an antagonist... 

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